Atherosclerotic
Plaque Rupture in
Humans and Mice

Jacques
Ohayon, PhD

Elucidating
atherosclertic
vulnerable plaque rupture by modeling
cross substitution of ApoE-/-
mouse and human plaque component stiffnesses- Biomechanics and Modeling in Mechanobiology. (in press), 2011 -The structure of mouse atherosclerotic lesions
may differ from that of humans, and mouse atherosclerotic plaque do not
rupture
except in some specific locations such as the brachiocephalic
artery. Recently, our group was the first to observe that the
amplitudes of in
vivo stresses in ApoE-/-
mouse aortic
atherosclerotic lesions were much lower and differed from those found
in a
previous work performed on human lesions. In this previous preliminary
work, we
hypothesized that the plaque mechanical properties (MP) may in turn be
responsible
for such species differences. However, the limited number of human
samples used
in our previous comparative study was relevant but not sufficient to
broadly
validate such hypothesis. Therefore, in this study, we propose an original finite element strategy that
reconstructs the in vivo
stress/strain (IVS/S) distributions in ApoE-/-
artherosclerotic
vessel based on cross substitution
of ApoE-/-
mouse and human plaque
components stiffnesses and
including residual stress/strain (RS/S). Our results: 1)
showed that
including RS/S decreases by a factor 2 the amplitude of maximal IVS/S,
and more
importantly 2) demonstrated that the
MP of the ApoE-/-
plaque constituents are mainly
responsible for the low level - compared to human - of intraplaque
stress in ApoE-/-
mouse aortic
atherosclerotic lesions (8.362.63
kPaversus
182.2555.88
kPa for human). Our study highlights that such
differences in
the distribution and amplitude of vessel wall stress might be one key
feature
for explaining for the difference in lesion stability between human
coronary
and mouse aortic lesions.